One of the most common eye disorders, dry eye disease, causes irritation or discomfort, and can decrease functional vision, sometimes causing a dramatic deterioration in the quality of life. About five million Americans over age 50 suffer from moderate-to-severe dry eyes, and tens of millions more have mild or episodic manifestations of the disease, at a cost of more than $50 billion.

In terms of treatment, there are several drops and drugs that can help. We spend hundreds of millions of dollars on things like artificial tears, but currently there is no therapy available to actually fix the problem. If drugs don't work, doctors can try plugging up the outflow tear ducts, but that can cause complications, such as plugs migrating and eroding into the face, requiring surgical removal. Alternatively, surgeons can just cauterize or stitch up the ducts in the first place.

There has to be a better way.

What about prevention? Dry eyes can be caused by LASIK surgery, affecting about 20-40% of patients six months after the operation. With a million LASIK procedures performed annually, that's a lot of people, and sometimes the long-term symptoms can be severe and disabling.

There's a long list of drugs that can cause it, including antihistamines, decongestants, nearly all the antidepressants, anticonvulsants, antipsychotics, anti-Parkinson's drugs, beta-blockers, and hormone replacement therapy, as well as a few herbal preparations.

In the developing world, vitamin A deficiency can start out as dry eyes and then progress to becoming the leading cause of preventable childhood blindness. Vitamin A deficiency is almost never seen in the developed world, unless you do it intentionally. There was a report in the 1960s of a guy who deliberately ate a vitamin A-deficient diet, living off of bread and lime juice for five years, and his eyes developed vascularization and ulceration of the cornea, which you can see (if you dare) in my Treating Dry Eye Disease with Diet: Just Add Water?video.That was better than what happened to an unfortunate woman who was the member of a cult and tried to live off of brown rice and herbal tea: Her eyes literally melted and collapsed.

There are also a couple case reports of autistic children who refused to eat anything but French fries or menus exclusively comprised of bacon, blueberry muffins, and Kool-Aid, and became vitamin A deficient. A case in the Bronx was written up as vegan diet and vitamin A deficiency, but it had nothing to do with his vegan diet--the kid refused to eat vegetables, consuming only potato chips, puffed rice cereal with non-fortified soymilk, and juice drinks. "His parents lacked particular skill in overcoming the child's tendency to avoid fruits and vegetables."

A plant-based diet may actually be the best thing for patients with dry eye disease, those who wear contact lenses, and those who wish to maximize their tear secretions. People with dry eyes should be advised to lower protein, total fat, and cholesterol intake, and do the following:

We know dehydration can cause a dry mouth, but could dehydration cause dry eyes? It may seem kind of obvious, but evidently it was never studied until recently. Is the answer to just drink more water? We know that those suffering from dry eye are comparatively dehydrated, so researchers figured that tear secretion decreases with progressive dehydration just like saliva secretion decreases and gives us a dry mouth. And indeed, as one gets more and more dehydrated, their urine concentrates and so does the tear fluid. But one can reverse that with rehydration, raising the exciting prospect that improving whole-body hydration by getting people to drink more water might bring relief for those with dry eyes. The researchers recommend eight cups of water a day for women and ten cups a day for men.

One of the most common eye disorders, dry eye disease, causes irritation or discomfort, and can decrease functional vision, sometimes causing a dramatic deterioration in the quality of life. About five million Americans over age 50 suffer from moderate-to-severe dry eyes, and tens of millions more have mild or episodic manifestations of the disease, at a cost of more than $50 billion.

In terms of treatment, there are several drops and drugs that can help. We spend hundreds of millions of dollars on things like artificial tears, but currently there is no therapy available to actually fix the problem. If drugs don't work, doctors can try plugging up the outflow tear ducts, but that can cause complications, such as plugs migrating and eroding into the face, requiring surgical removal. Alternatively, surgeons can just cauterize or stitch up the ducts in the first place.

There has to be a better way.

What about prevention? Dry eyes can be caused by LASIK surgery, affecting about 20-40% of patients six months after the operation. With a million LASIK procedures performed annually, that's a lot of people, and sometimes the long-term symptoms can be severe and disabling.

There's a long list of drugs that can cause it, including antihistamines, decongestants, nearly all the antidepressants, anticonvulsants, antipsychotics, anti-Parkinson's drugs, beta-blockers, and hormone replacement therapy, as well as a few herbal preparations.

In the developing world, vitamin A deficiency can start out as dry eyes and then progress to becoming the leading cause of preventable childhood blindness. Vitamin A deficiency is almost never seen in the developed world, unless you do it intentionally. There was a report in the 1960s of a guy who deliberately ate a vitamin A-deficient diet, living off of bread and lime juice for five years, and his eyes developed vascularization and ulceration of the cornea, which you can see (if you dare) in my Treating Dry Eye Disease with Diet: Just Add Water?video.That was better than what happened to an unfortunate woman who was the member of a cult and tried to live off of brown rice and herbal tea: Her eyes literally melted and collapsed.

There are also a couple case reports of autistic children who refused to eat anything but French fries or menus exclusively comprised of bacon, blueberry muffins, and Kool-Aid, and became vitamin A deficient. A case in the Bronx was written up as vegan diet and vitamin A deficiency, but it had nothing to do with his vegan diet--the kid refused to eat vegetables, consuming only potato chips, puffed rice cereal with non-fortified soymilk, and juice drinks. "His parents lacked particular skill in overcoming the child's tendency to avoid fruits and vegetables."

A plant-based diet may actually be the best thing for patients with dry eye disease, those who wear contact lenses, and those who wish to maximize their tear secretions. People with dry eyes should be advised to lower protein, total fat, and cholesterol intake, and do the following:

We know dehydration can cause a dry mouth, but could dehydration cause dry eyes? It may seem kind of obvious, but evidently it was never studied until recently. Is the answer to just drink more water? We know that those suffering from dry eye are comparatively dehydrated, so researchers figured that tear secretion decreases with progressive dehydration just like saliva secretion decreases and gives us a dry mouth. And indeed, as one gets more and more dehydrated, their urine concentrates and so does the tear fluid. But one can reverse that with rehydration, raising the exciting prospect that improving whole-body hydration by getting people to drink more water might bring relief for those with dry eyes. The researchers recommend eight cups of water a day for women and ten cups a day for men.

The relative paralysis of our arteries for hours after eating fast food and cheesecake may also occur after consuming olive oil. Olive oil was found to have the same impairment to endothelial function as high-fat foods like sausage and egg breakfast sandwiches. (See my Olive Oil and Artery Functionvideo for an illustrative chart with different foods.)

Studies that have suggested endothelial benefits after olive oil consumption have measured something different: ischemia-induced dilation as opposed to flow-mediated dilation. There's just not good evidence that's actually an accurate index of endothelial function, which is what predicts heart disease. Hundreds of studies have shown that the ischemia-induced dilation test can give a false negative result.

Other oils have also been shown to have deleterious results on endothelial function. A significant and constant decrease in endothelial function appears within three hours after each meal, independent of the type of oil and whether the oil was fresh or deep fried. Olive oil may be better than omega-6-rich oils or saturated fats, but it still showed adverse effects. This was the case with regular, refined olive oil. But what about extra-virgin olive oil?

Extra-virgin olive oil retains a fraction of the anti-inflammatory phytonutrients found in the olive fruit, and so doesn't appear to induce the spike in inflammatory markers caused by regular olive oil. What does that mean for our arteries? Extra-virgin olive oil may have more of a neutral effect compared to butter, which exerted a noxious effect that lasted for up to six hours--basically right up until our next meal. In the largest prospective study ever to assess the relationship between olive oil consumption and cardiac events like heart attacks, there was a suggestion that virgin olive oil may be better than regular olive oil, but neither was found to significantly reduce heart attack rates after controlling for healthy dietary behaviors like vegetable intake, which tends to go hand-in-hand with olive oil intake.

There have also been studies showing that even extra-virgin olive oil, contrary to expectations, may significantly impair endothelial function. Why then do some studies suggest endothelial function improves on a Mediterranean diet, which is rich in olive oil? It may be because the Mediterranean diet is also rich in whole grains, fruits, vegetables, beans, and walnuts. Fruits and vegetables appear to provide some protection against the direct impairment of endothelial function produced by high-fat foods, including olive oil; therefore, improvements in health may be in spite of, rather than because of, the oil. In terms of their effects on post-meal endothelial function, the beneficial components of the Mediterranean diet may primarily be the antioxidant-rich foods, the vegetables, fruits, and their derivatives, such as balsamic vinegar. Adding some vegetables to a fatty meal may partially restore arterial functioning and blood flow.

The relative paralysis of our arteries for hours after eating fast food and cheesecake may also occur after consuming olive oil. Olive oil was found to have the same impairment to endothelial function as high-fat foods like sausage and egg breakfast sandwiches. (See my Olive Oil and Artery Functionvideo for an illustrative chart with different foods.)

Studies that have suggested endothelial benefits after olive oil consumption have measured something different: ischemia-induced dilation as opposed to flow-mediated dilation. There's just not good evidence that's actually an accurate index of endothelial function, which is what predicts heart disease. Hundreds of studies have shown that the ischemia-induced dilation test can give a false negative result.

Other oils have also been shown to have deleterious results on endothelial function. A significant and constant decrease in endothelial function appears within three hours after each meal, independent of the type of oil and whether the oil was fresh or deep fried. Olive oil may be better than omega-6-rich oils or saturated fats, but it still showed adverse effects. This was the case with regular, refined olive oil. But what about extra-virgin olive oil?

Extra-virgin olive oil retains a fraction of the anti-inflammatory phytonutrients found in the olive fruit, and so doesn't appear to induce the spike in inflammatory markers caused by regular olive oil. What does that mean for our arteries? Extra-virgin olive oil may have more of a neutral effect compared to butter, which exerted a noxious effect that lasted for up to six hours--basically right up until our next meal. In the largest prospective study ever to assess the relationship between olive oil consumption and cardiac events like heart attacks, there was a suggestion that virgin olive oil may be better than regular olive oil, but neither was found to significantly reduce heart attack rates after controlling for healthy dietary behaviors like vegetable intake, which tends to go hand-in-hand with olive oil intake.

There have also been studies showing that even extra-virgin olive oil, contrary to expectations, may significantly impair endothelial function. Why then do some studies suggest endothelial function improves on a Mediterranean diet, which is rich in olive oil? It may be because the Mediterranean diet is also rich in whole grains, fruits, vegetables, beans, and walnuts. Fruits and vegetables appear to provide some protection against the direct impairment of endothelial function produced by high-fat foods, including olive oil; therefore, improvements in health may be in spite of, rather than because of, the oil. In terms of their effects on post-meal endothelial function, the beneficial components of the Mediterranean diet may primarily be the antioxidant-rich foods, the vegetables, fruits, and their derivatives, such as balsamic vinegar. Adding some vegetables to a fatty meal may partially restore arterial functioning and blood flow.

Botanically speaking, seeds are small embryonic plants--the whole plant stuffed into a tiny seed and surrounded by an outer layer packed with vitamins, minerals, and phytochemicals to protect the seedling plant's DNA from free radicals. No wonder they're so healthy. By seeds, using the formal definition, we're talking all whole grains; grains are seeds--you plant them and they grow. Nuts are just dry fruits with one or two seeds. Legumes (beans, peas, and lentils) are seeds, too, as are cocoa and coffee beans. So, finding health-promoting effects in something like cocoa or coffee should not be all that surprising. There is substantial evidence that increased consumption of all these little plants is associated with lower risk of cardiovascular disease.

Of course, much of chocolate research is just on how to get consumers to eat more. While it didn't seem to matter what kind of music people were listening to when it came to the flavor intensity, pleasantness, or texture of a bell pepper, people liked chocolate more when listening to jazz than classical, rock, or hip hop. Why is this important? So food industries can "integrate specific musical stimuli" in order to maximize their profits. For example, purveyors may play jazz in the background to increase consumers' acceptance of their chocolates. Along these lines, another study demonstrated that people rated the oyster eaten "more pleasant in the presence of the 'sound of the sea' than in the presence of 'farmyard noises.'"

You'd think chocolate would just sell itself, given that it's considered the most commonly craved food in the world. The same degree of interest doesn't seem to exist as to whether or not Brussels sprouts might provide similar cardiovascular protection. So, it's understandable to hope chocolate provides health benefits. Meanwhile, despite their known benefits, Brussels sprouts don't get the love they deserve.

One of the potential downsides of chocolate is weight gain, which is the subject of my Does Chocolate Cause Weight Gain? video. Though cocoa hardly has any calories, chocolate is one of the most calorie-dense foods. For example: A hundred calories of chocolate is less than a quarter of a bar, compared to a hundred calories of strawberries, which is more than two cups..

A few years ago, a study funded by the National Confectioners Association--an organization that, among other things, runs the website voteforcandy.com--reported that Americans who eat chocolate weigh, on average, four pounds less than those who don't. But maybe chocolate-eaters exercise more or eat more fruits and vegetables. The researchers didn't control for any of that.

The findings of a more recent study published in the Archives of Internal Medicine were less easy to dismiss and there were no apparent ties to Big Chocolate. The researchers reported that out of a thousand men and women they studied in San Diego, those who frequently consumed chocolate had a lower BMI--actually weighed less--than those who ate chocolate less often. And this was even after adjusting for physical activity and diet quality. But, it was a cross-sectional study, meaning a snapshot in time, so you can't prove cause and effect. Maybe not eating chocolate leads to being fatter, or maybe being fatter leads to not eating chocolate. Maybe people who are overweight are trying to cut down on sweets. What we need is a study in which people are followed over time.

There was no such prospective study, until now. More than 10,000 people were followed for six years, and a chocolate habit was associated with long-term weight gain in a dose-response manner. This means the greatest weight gain over time was seen in those with the highest frequency of chocolate intake. It appears the reason the cross-sectional studies found the opposite is that subjects diagnosed with obesity-related illnesses tended to reduce their intake of things like chocolate in an attempt to improve their prognosis. This explains why heavier people may, on average, eat less chocolate.

To bolster this finding came the strongest type of evidence--an interventional trial--in which you split people up into two groups and change half their diets. Indeed, adding four squares of chocolate to peoples' daily diets does appear to add a few pounds.

So, what do we tell our patients? In 2013, researchers wrote in the American Family Physician journal that "because many cocoa products are high in sugar and saturated fat, family physicians should refrain from recommending cocoa...." That's a little patronizing, though. You can get the benefits of chocolate without any sugar or fat by adding cocoa powder to a smoothie, for example. Too often, doctors think patients can't handle the truth. Case in point: If your patients inquire, one medical journal editorial suggest, ask them what type of chocolate they prefer. If they respond with milk chocolate, then it is best to answer that it is not good for them. If the answer is dark chocolate, then you can lay out the evidence.

Botanically speaking, seeds are small embryonic plants--the whole plant stuffed into a tiny seed and surrounded by an outer layer packed with vitamins, minerals, and phytochemicals to protect the seedling plant's DNA from free radicals. No wonder they're so healthy. By seeds, using the formal definition, we're talking all whole grains; grains are seeds--you plant them and they grow. Nuts are just dry fruits with one or two seeds. Legumes (beans, peas, and lentils) are seeds, too, as are cocoa and coffee beans. So, finding health-promoting effects in something like cocoa or coffee should not be all that surprising. There is substantial evidence that increased consumption of all these little plants is associated with lower risk of cardiovascular disease.

Of course, much of chocolate research is just on how to get consumers to eat more. While it didn't seem to matter what kind of music people were listening to when it came to the flavor intensity, pleasantness, or texture of a bell pepper, people liked chocolate more when listening to jazz than classical, rock, or hip hop. Why is this important? So food industries can "integrate specific musical stimuli" in order to maximize their profits. For example, purveyors may play jazz in the background to increase consumers' acceptance of their chocolates. Along these lines, another study demonstrated that people rated the oyster eaten "more pleasant in the presence of the 'sound of the sea' than in the presence of 'farmyard noises.'"

You'd think chocolate would just sell itself, given that it's considered the most commonly craved food in the world. The same degree of interest doesn't seem to exist as to whether or not Brussels sprouts might provide similar cardiovascular protection. So, it's understandable to hope chocolate provides health benefits. Meanwhile, despite their known benefits, Brussels sprouts don't get the love they deserve.

One of the potential downsides of chocolate is weight gain, which is the subject of my Does Chocolate Cause Weight Gain? video. Though cocoa hardly has any calories, chocolate is one of the most calorie-dense foods. For example: A hundred calories of chocolate is less than a quarter of a bar, compared to a hundred calories of strawberries, which is more than two cups..

A few years ago, a study funded by the National Confectioners Association--an organization that, among other things, runs the website voteforcandy.com--reported that Americans who eat chocolate weigh, on average, four pounds less than those who don't. But maybe chocolate-eaters exercise more or eat more fruits and vegetables. The researchers didn't control for any of that.

The findings of a more recent study published in the Archives of Internal Medicine were less easy to dismiss and there were no apparent ties to Big Chocolate. The researchers reported that out of a thousand men and women they studied in San Diego, those who frequently consumed chocolate had a lower BMI--actually weighed less--than those who ate chocolate less often. And this was even after adjusting for physical activity and diet quality. But, it was a cross-sectional study, meaning a snapshot in time, so you can't prove cause and effect. Maybe not eating chocolate leads to being fatter, or maybe being fatter leads to not eating chocolate. Maybe people who are overweight are trying to cut down on sweets. What we need is a study in which people are followed over time.

There was no such prospective study, until now. More than 10,000 people were followed for six years, and a chocolate habit was associated with long-term weight gain in a dose-response manner. This means the greatest weight gain over time was seen in those with the highest frequency of chocolate intake. It appears the reason the cross-sectional studies found the opposite is that subjects diagnosed with obesity-related illnesses tended to reduce their intake of things like chocolate in an attempt to improve their prognosis. This explains why heavier people may, on average, eat less chocolate.

To bolster this finding came the strongest type of evidence--an interventional trial--in which you split people up into two groups and change half their diets. Indeed, adding four squares of chocolate to peoples' daily diets does appear to add a few pounds.

So, what do we tell our patients? In 2013, researchers wrote in the American Family Physician journal that "because many cocoa products are high in sugar and saturated fat, family physicians should refrain from recommending cocoa...." That's a little patronizing, though. You can get the benefits of chocolate without any sugar or fat by adding cocoa powder to a smoothie, for example. Too often, doctors think patients can't handle the truth. Case in point: If your patients inquire, one medical journal editorial suggest, ask them what type of chocolate they prefer. If they respond with milk chocolate, then it is best to answer that it is not good for them. If the answer is dark chocolate, then you can lay out the evidence.

Until about ten years ago, brown adipose tissue (BAT) was considered to be biologically active only in babies and small children where it generates heat by burning fat. But now, there is no doubt that active brown fat is present in adult humans and is involved in cold-induced increases in whole-body calorie expenditure and, thereby, helps control of not only body temperature but also how fat we are.

In 2013, researchers showed that one could activate brown adipose tissue if you chill out people long enough, specifically, by exposing them to two hours of cold every day for six weeks, which can lead to a significant reduction in body fat. You can see an illustrative graph in my video Boosting Brown Fat Through Diet. Although researchers demonstrated the effective recruitment of human brown fat, it would seem difficult to increase exposure to cold in daily life. Thankfully, our brown fat can also be activated by some food ingredients, such as capsaicin, the compound that makes hot peppers hot.

While physical activity is usually recommended to increase energy expenditure, there are specific food components, such as capsaicin, that are known to burn off calories. For example, one study found that there was a significant rise in energy expenditure within 30 minutes of eating the equivalent of a jalapeño pepper.

Normally when we cut down on calories, our metabolism slows down, undercutting our weight loss attempts; but sprinkling a third of a teaspoon of red chili pepper powder onto our meals counteracts that metabolic slow down and promotes fat burning. Researchers wanted to try giving participants more chili pepper in order to try to match some of the studies done in Asia, but the Caucasian subjects couldn't take it. But by adding more than a tablespoon of red pepper powder to a high-fat meal, Japanese women burned significantly more fat.

We've known for decades that cayenne pepper increases metabolic rate, but we didn't know how. But studies show that this class of compounds increases energy expenditure in human individuals with brown fat, but not in those without it, indicating that individuals increase expenditure right off the BAT. Additionally, there is a variety of structurally similar flavor molecules in other foods, like black pepper and ginger, that may activate thermogenesis as well, but they haven't been directly tested.

All these results suggest that the anti-obesity effects of pepper compounds are based on the heat-generating activity of recruited brown fat. Thus, repeated ingestion can mimic the chronic effects of cold exposure without having to freeze ourselves.

Consumption of spicy foods may help us lose weight, but what about the sensory burn and pain on our tongues and sometimes in our stomachs as well as further on down? Are our only two options for boosting brown fat to freeze our legs or burn our butts?

Arginine-rich foods may also stimulate brown adipose tissue growth and development through a variety of mechanisms, which is achieved by consuming more soy foods, seeds, nuts, and beans.

Until about ten years ago, brown adipose tissue (BAT) was considered to be biologically active only in babies and small children where it generates heat by burning fat. But now, there is no doubt that active brown fat is present in adult humans and is involved in cold-induced increases in whole-body calorie expenditure and, thereby, helps control of not only body temperature but also how fat we are.

In 2013, researchers showed that one could activate brown adipose tissue if you chill out people long enough, specifically, by exposing them to two hours of cold every day for six weeks, which can lead to a significant reduction in body fat. You can see an illustrative graph in my video Boosting Brown Fat Through Diet. Although researchers demonstrated the effective recruitment of human brown fat, it would seem difficult to increase exposure to cold in daily life. Thankfully, our brown fat can also be activated by some food ingredients, such as capsaicin, the compound that makes hot peppers hot.

While physical activity is usually recommended to increase energy expenditure, there are specific food components, such as capsaicin, that are known to burn off calories. For example, one study found that there was a significant rise in energy expenditure within 30 minutes of eating the equivalent of a jalapeño pepper.

Normally when we cut down on calories, our metabolism slows down, undercutting our weight loss attempts; but sprinkling a third of a teaspoon of red chili pepper powder onto our meals counteracts that metabolic slow down and promotes fat burning. Researchers wanted to try giving participants more chili pepper in order to try to match some of the studies done in Asia, but the Caucasian subjects couldn't take it. But by adding more than a tablespoon of red pepper powder to a high-fat meal, Japanese women burned significantly more fat.

We've known for decades that cayenne pepper increases metabolic rate, but we didn't know how. But studies show that this class of compounds increases energy expenditure in human individuals with brown fat, but not in those without it, indicating that individuals increase expenditure right off the BAT. Additionally, there is a variety of structurally similar flavor molecules in other foods, like black pepper and ginger, that may activate thermogenesis as well, but they haven't been directly tested.

All these results suggest that the anti-obesity effects of pepper compounds are based on the heat-generating activity of recruited brown fat. Thus, repeated ingestion can mimic the chronic effects of cold exposure without having to freeze ourselves.

Consumption of spicy foods may help us lose weight, but what about the sensory burn and pain on our tongues and sometimes in our stomachs as well as further on down? Are our only two options for boosting brown fat to freeze our legs or burn our butts?

Arginine-rich foods may also stimulate brown adipose tissue growth and development through a variety of mechanisms, which is achieved by consuming more soy foods, seeds, nuts, and beans.

Depression is a serious and common mental disorder responsible for the majority of suicides. As I've covered in Antioxidants & Depression, intake of fruits, vegetables, and naturally occurring antioxidants have been found to be protectively associated with depression. Therefore, researchers have considered that "it may be possible to prevent depression or to lessen its negative effects through dietary intervention."

But not so fast. Cross-sectional studies are snapshots in time, so we don't know "whether a poor dietary pattern precedes the development of depression or if depression causes poor dietary intake." Depression and even treatments for depression can affect appetite and dietary intake. Maybe people who feel crappier just eat crappier, instead of the other way around.

What we need is a prospective study (a study performed over time) where we start out with people who are not depressed and follow them for several years. In 2012, we got just such a study, which ran over six years. As you'll see in my video Fish Consumption and Suicide, those with higher carotenoid levels in their bloodstream, which is considered a good indicator of fruit and vegetable intake, had a 28% lower risk of becoming depressed within that time. The researchers conclude that having low blood levels of those healthy phytonutrients may predict the development of new depressive symptoms. What about suicide?

Worldwide, a million people kill themselves every year. Of all European countries, Greece appears to have the lowest rates of suicide. It may be the balmy weather, but it may also have something to do with their diet. Ten thousand people were followed for years, and those following a more Mediterranean diet pattern were less likely to be diagnosed with depression. What was it about the diet that was protective? It wasn't the red wine or fish; it was the fruit, nuts, beans, and effectively higher plant to animal fat ratio that appeared protective. Conversely, significant adverse trends were observed for dairy and meat consumption.

A similar protective dietary pattern was found in Japan. A high intake of vegetables, fruits, mushrooms, and soy products was associated with a decreased prevalence of depressive symptoms. The healthy dietary pattern was not characterized by a high intake of seafood. Similar results were found in a study of 100,000 Japanese men and women followed for up to 10 years. There was no evidence of a protective role of higher fish consumption or the long-chain omega 3s EPA and DHA against suicide. In fact, they found a significantly increasedrisk of suicide among male nondrinkers with high seafood omega 3 intake. This may have been by chance, but a similar result was found in the Mediterranean. High baseline fish consumption with an increase in consumption were associated with an increased risk of mental disorders.

One possible explanation could be the mercury content of fish. Could an accumulation of mercury compounds in the body increase the risk of depression? We know that mercury in fish can cause neurological damage, associated with increased risk of Alzheimer's disease, memory loss, and autism, but also depression. Therefore, "the increased risk of suicide among persons with a high fish intake might also be attributable to the harmful effects of mercury in fish."

Large Harvard University cohort studies found similar results. Hundreds of thousands were followed for up to 20 years, and no evidence was found that taking fish oil or eating fish lowered risk of suicide. There was even a trend towards higher suicide mortality.

What about fish consumption for the treatment of depression? When we put together all the trials done to date, neither the EPA nor DHA long-chain omega-3s appears more effective than sugar pills. We used to think omega-3 supplementation was useful, but several recent studies have tipped the balance the other way. It seems that "[n]early all of the treatment efficacy observed in the published literature may be attributable to publication bias," meaning the trials that showed no benefit tended not to get published at all. So, all doctors saw were a bunch of positive studies, but only because a bunch of the negative ones were buried.

What about antidepressant drugs? Sometimes they can be absolutely life-saving, but other times they may actually do more harm than good. See my controversial video Do Antidepressant Drugs Really Work?.

Depression is a serious and common mental disorder responsible for the majority of suicides. As I've covered in Antioxidants & Depression, intake of fruits, vegetables, and naturally occurring antioxidants have been found to be protectively associated with depression. Therefore, researchers have considered that "it may be possible to prevent depression or to lessen its negative effects through dietary intervention."

But not so fast. Cross-sectional studies are snapshots in time, so we don't know "whether a poor dietary pattern precedes the development of depression or if depression causes poor dietary intake." Depression and even treatments for depression can affect appetite and dietary intake. Maybe people who feel crappier just eat crappier, instead of the other way around.

What we need is a prospective study (a study performed over time) where we start out with people who are not depressed and follow them for several years. In 2012, we got just such a study, which ran over six years. As you'll see in my video Fish Consumption and Suicide, those with higher carotenoid levels in their bloodstream, which is considered a good indicator of fruit and vegetable intake, had a 28% lower risk of becoming depressed within that time. The researchers conclude that having low blood levels of those healthy phytonutrients may predict the development of new depressive symptoms. What about suicide?

Worldwide, a million people kill themselves every year. Of all European countries, Greece appears to have the lowest rates of suicide. It may be the balmy weather, but it may also have something to do with their diet. Ten thousand people were followed for years, and those following a more Mediterranean diet pattern were less likely to be diagnosed with depression. What was it about the diet that was protective? It wasn't the red wine or fish; it was the fruit, nuts, beans, and effectively higher plant to animal fat ratio that appeared protective. Conversely, significant adverse trends were observed for dairy and meat consumption.

A similar protective dietary pattern was found in Japan. A high intake of vegetables, fruits, mushrooms, and soy products was associated with a decreased prevalence of depressive symptoms. The healthy dietary pattern was not characterized by a high intake of seafood. Similar results were found in a study of 100,000 Japanese men and women followed for up to 10 years. There was no evidence of a protective role of higher fish consumption or the long-chain omega 3s EPA and DHA against suicide. In fact, they found a significantly increasedrisk of suicide among male nondrinkers with high seafood omega 3 intake. This may have been by chance, but a similar result was found in the Mediterranean. High baseline fish consumption with an increase in consumption were associated with an increased risk of mental disorders.

One possible explanation could be the mercury content of fish. Could an accumulation of mercury compounds in the body increase the risk of depression? We know that mercury in fish can cause neurological damage, associated with increased risk of Alzheimer's disease, memory loss, and autism, but also depression. Therefore, "the increased risk of suicide among persons with a high fish intake might also be attributable to the harmful effects of mercury in fish."

Large Harvard University cohort studies found similar results. Hundreds of thousands were followed for up to 20 years, and no evidence was found that taking fish oil or eating fish lowered risk of suicide. There was even a trend towards higher suicide mortality.

What about fish consumption for the treatment of depression? When we put together all the trials done to date, neither the EPA nor DHA long-chain omega-3s appears more effective than sugar pills. We used to think omega-3 supplementation was useful, but several recent studies have tipped the balance the other way. It seems that "[n]early all of the treatment efficacy observed in the published literature may be attributable to publication bias," meaning the trials that showed no benefit tended not to get published at all. So, all doctors saw were a bunch of positive studies, but only because a bunch of the negative ones were buried.

What about antidepressant drugs? Sometimes they can be absolutely life-saving, but other times they may actually do more harm than good. See my controversial video Do Antidepressant Drugs Really Work?.